By either oral or subcutaneous administration of glutamate (GLU) to various animal species, it is possible to destroy certain CNS neurons which are accessible to GLU from blood. Since various neuroexcitatory structural analogues of GLU readily reproduce this type of brain damage, this family of GLU analogues has been referred to as the excitotoxic amino acids, the assumption being that their toxic effect on central neurons is an exaggerated expression of their excitatory effect. Another common amino acid, L-cysteine, induces a pattern of brain damage in infant or fetal rodents when administered either orally or subcutaneously, which is different from and more widespread than that induced by excitotoxic amino acids. The mechanism of cysteine-induced brain damage remains obscure. Renewal of support is requested herein for ongoing ultrastructural, neuro-chemical and toxipharmacological studies aimed at further clarifying the mechanisms underlying the neurotoxic potential both of cysteine and the excitotoxic amino acids and at determining what relevance such mechanisms may have to human CNS disease.